Rad51-deficient vertebrate cells accumulate chromosomal breaks prior to cell death

被引：687

作者：

Sonoda, E

Sasaki, MS

Buerstedde, JM

Bezzubova, O

Shinohara, A

Ogawa, H

Takata, M

Yamaguchi-Iwai, Y

Takeda, S

机构：

[1] Kyoto Univ, Fac Med, Dept Mol Immunol & Allergiol, Sakyo Ku, Kyoto 60601, Japan

[2] Kyoto Univ, Ctr Radiat Biol, Sakyo Ku, Kyoto 60601, Japan

[3] Basel Inst Immunol, CH-4005 Basel, Switzerland

[4] Osaka Univ, Grad Sch Sci, Dept Biol, Osaka 560, Japan

来源：

EMBO JOURNAL | 1998年 / 17卷 / 02期

关键词：

chromosome aberration; DT40; double-strand break; Rad51; disruption;

D O I：

10.1093/emboj/17.2.598

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Yeast rad51 mutants are viable, but extremely sensitive to gamma-rays due to defective repair of double-strand breaks, In contrast, disruption of the murine RAD51 homologue is lethal, indicating an essential role of Rad51 in vertebrate cells. We generated clones of the chicken B lymphocyte line DT40 carrying a human RAD51 transgene under the control of a repressible promoter and subsequently disrupted the endogenous RAD51 loci, Upon inhibition of the RAD51 transgene, Rad51(-) cells accumulated in the G(2)/M phase of the cell cycle before dying. Chromosome analysis revealed that most metaphase-arrested Rad51(-) cells carried isochromatid-type breaks, In conclusion, Rad51 fulfils an essential role in the repair of spontaneously occurring chromosome breaks in proliferating cells of higher eukaryotes.

引用

页码：598 / 608

页数：11

共 76 条

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